Purulent Bacterial Pericarditis Complicated by Cardiac Tamponade and Effusive Constrictive Pericarditis

Abstract

Background

Purulent pericarditis is a rare but severe presentation of acute pericarditis that can rapidly progress to effusive-constrictive pericarditis (ECP), a syndrome characterized by concomitant cardiac tamponade and constrictive pericarditis.

Case Summary

A 62-year-old woman with diabetes presented with chills, dyspnea, and pleuritic chest pain. Despite initial treatment for idiopathic acute pericarditis, she rapidly developed cardiac tamponade. Emergent pericardiocentesis yielded purulent fluid consistent with Streptococcus pneumoniae pericarditis, and postdrainage echocardiogram demonstrated constrictive physiology, supporting a diagnosis of ECP. The patient subsequently underwent partial pericardiectomy, with marked clinical improvement.

Discussion

This case highlights the rapid progression of nontuberculous purulent pericarditis to ECP and underscores the importance of serial echocardiography in diagnosing, monitoring, and managing ECP.

Take-Home Messages

ECP is a rare but under-recognized complication of purulent pericarditis, requiring a high clinical suspicion. Given the diagnostic challenges, early recognition, close monitoring, and timely intervention are critical to improving outcomes.

Graphical Abstract

History of Presentation

A 62-year-old woman presented to the emergency department with a few days of chills, myalgias, and new-onset chest pain associated with shortness of breath. Upon arrival, she was afebrile, with sinus tachycardia at 130 beats/min, normotensive with a blood pressure of 100/77 mm Hg, tachypneic with a respiratory rate of 24 breaths/min, and had an oxygen saturation of 98% on 2 L of nasal cannula. Physical examination revealed decreased left lower lobe lung sounds. Laboratory work-up showed leukocytosis (15,000 cells/μL), hemoglobin within baseline (11.7 g/dL), mildly elevated creatinine (1.05 mg/dL), mildly elevated high-sensitivity troponin (34 ng/dL), elevated hemoglobin A1c (8.5%), and elevated C-reactive protein (606 mg/dL) and erythrocyte sedimentation rate (58 mm/h). Chest x-ray revealed a dense left retrocardiac airspace opacity. Initial electrocardiogram showed ST-segment elevations in leads I, aVL, V5, and V6. Given concern for ST-elevation myocardial infarction, emergent coronary angiography was performed, revealing nonobstructive epicardial coronary artery disease. The patient was admitted to the medical intensive care unit.

Take-Home Messages

• •Effusive-constrictive pericarditis is a rare but under-recognized complication of purulent pericarditis, requiring high clinical suspicion and timely intervention.
• •Serial echocardiographic monitoring pre- and postpericardiocentesis may aid in early detection of constrictive physiology, potentially guiding treatment decisions and improving patient prognosis.

Past Medical History

The patient had a history of poorly controlled type 2 diabetes mellitus and hypertension. Her home medications included metformin, glipizide, lisinopril, and gabapentin. One month before admission, her hemoglobin A1c was elevated at 9.3%. She denied any recent surgeries or interventions. She was a former tobacco smoker, with the last cigarette 30 years before presentation, and she denied any history of alcohol or intravenous drug use.

Differential Diagnosis

The patient's presentation was initially suggestive of community-acquired pneumonia. However, given presence of ST-segment elevation on electrocardiogram, myocarditis, pericarditis, and stress cardiomyopathy were among the top considerations. Other possibilities included sepsis-induced myocardial dysfunction, pulmonary embolism, and coronary vasospasm.

Investigations

After the coronary angiogram, a computed tomography angiogram of the chest showed no evidence of pulmonary embolism but revealed a large pericardial effusion. Transthoracic echocardiogram (TTE) demonstrated normal left ventricular systolic function and a moderate-sized circumferential pericardial effusion without hemodynamic compromise. Further work-up for pericarditis included an unremarkable respiratory viral panel, negative blood cultures, and normal autoimmune/inflammatory markers (antinuclear antibody, cyclic citrullinated peptide, rheumatoid factor, perinuclear antineutrophil cytoplasmic antibody, myeloperoxidase antibody). Blood urea nitrogen was normal (18 mg/dL), and thyroid-stimulating hormone was mildly decreased (0.152 uIU/mL) but with free thyroxine levels within normal limits (0.9 ng/dL). A urine drug screen was positive for marijuana. The patient was initially treated as having idiopathic acute pericarditis and was given colchicine and high-dose nonsteroidal anti-inflammatory drugs.

On hospital day 7, the patient developed acutely worsening dyspnea, hypotension (90s/50s), tachycardia (140-150s), and hypoxia requiring 4 L of supplemental oxygen, concerning for acute cardiac tamponade. Repeat TTE revealed an interval increase in the size of the pericardial effusion, associated with a dilated inferior vena cava (IVC) and prominent respirophasic tricuspid and mitral inflow velocity variation, supportive of tamponade physiology (Figure 1). Urgent pericardiocentesis was performed, returning 410 mL of purulent fluid with immediate improvement in hemodynamics, and a pericardial drain was placed. Given the suspicion of purulent pericarditis (PP), she was started on broad-spectrum antibiotics with piperacillin-tazobactam and vancomycin. Pericardial fluid cultures grew Streptococcus pneumoniae, and antibiotic treatment was switched to culture-guided intravenous ceftriaxone. Despite initial improvement, persistent sinus tachycardia and jugular venous distension prompted further investigation. Repeat TTE on hospital day 11 showed a small residual pericardial effusion but demonstrated new evidence of constrictive physiology, including annulus reversus (medial e′/lateral e′ ratio: 1.7), respirophasic tricuspid and mitral inflow velocity variation, diastolic expiratory flow reversal of the hepatic vein, and persistent IVC dilation, consistent with elevated right atrial (RA) pressures despite pericardial drainage (Figure 2). Repeat chest computed tomography also showed interval development of a large, loculated, left-sided pleural effusion (Figure 3).

Figure 1.

Limited Transthoracic Echocardiogram Concerning for Cardiac Tamponade

(A) A large, circumferential, free-flowing pericardial effusion. (B and C) Prominent respirophasic variation in tricuspid and mitral inflow velocities.

Figure 2.

Transthoracic Echocardiogram Demonstrating Constrictive Physiology

(A and B) Medial and lateral e′ velocities. (C and D) Prominent respirophasic variation in tricuspid and mitral inflow velocities. (E) Expiratory diastolic flow reversal in the hepatic vein.

Figure 3.

Noncontrast Computed Tomography of the Chest Revealing a Left-Sided Empyema Complicating a Complex Pericardial Effusion

(A) Axial plane and (B) frontal plane.

Management

The patient was diagnosed with effusive-constrictive pericarditis (ECP) and underwent left video-assisted thoracoscopic decortication with chest tube placement, along with a partial pericardiectomy. A significant amount of purulent and fibrinous material was debrided. The pathology of resected pericardium was suggestive of acute pericarditis with granulation tissue and fibrosis (Figure 4). Postsurgical TTE demonstrated resolution of constrictive physiology findings. Serial chest imaging demonstrated marked improvement in the left pleural effusion, and the left-sided chest tube was subsequently removed on postoperative day 10. The patient's postoperative recovery was uneventful, and she was discharged with a prolonged oral antibiotic regimen.

Figure 4.

Hematoxylin and Eosin Staining of Pericardial Tissue With Granulation and Fibrosis Consistent With Effusive-Constrictive Pericarditis (10× Magnification)

Discussion

The advent of antibiotics and vaccines have made bacterial infection an exceedingly rare cause of acute pericarditis in developed countries, occurring in approximately 1 in 18,000 patients. Because of its low index of suspicion and high mortality rate, the diagnosis is made postmortem in nearly half of cases.¹

We present a case of primary nontuberculous PP that rapidly progressed to ECP, a syndrome characterized by constrictive pericarditis coexisting with a hemodynamically significant pericardial effusion, resulting in tamponade. In developing countries, the most common cause of ECP is tuberculosis pericarditis, with reported incidence rates of 3% to 14%. Other etiologies of ECP include idiopathic, viral, postprocedural, neoplastic, traumatic, and postradiation, with reported incidences ranging from 2.4% to 14.8%.¹

A thorough literature review identified only 1 case of nontuberculous PP classified as ECP by its authors.² However, at least 2 additional case reports describe patients with nontuberculous PP who met the diagnostic criteria for ECP.^3,4 Although these cases demonstrated constrictive physiology and persistently elevated RA pressures after pericardiocentesis for tamponade, none explicitly referred to the syndrome as ECP, highlighting its potential underdiagnosis and underappreciation.

ECP can be difficult to diagnose, as its presentation can overlap with that of cardiac tamponade, and diagnosis has traditionally relied on invasive right heart catheterization to demonstrate persistently elevated RA pressures despite pericardiocentesis (>10 mm Hg or reduction of <50% from baseline).¹ However, simultaneous right heart catheterization during pericardiocentesis is no longer routinely performed, which may contribute to ECP being an under-recognized entity.

Modern echocardiography offers a more accessible and noninvasive diagnostic tool to distinguish ECP from other complications of PP, including cardiac tamponade. Both conditions demonstrate a hemodynamically significant pericardial effusion including ventricular interdependence, expiratory hepatic flow reversal, right-sided chamber collapse, and dilated IVC suggestive of elevated RA pressures. Yet, careful TTE interpretation may also reveal septal bounce, medial (septal) e′ velocity greater than lateral e′ velocity (ie, annulus reversus), paradoxical increase in mitral annular early diastolic velocity (ie, annulus paradoxus), elevated mitral E-wave velocity, an E/A ratio in expiration >1.6, and thickened pericardium suggestive of concomitant constrictive physiology more consistent with ECP (Table 1).^5,6 Notably, the absence of pericardial thickening is not sensitive for excluding constrictive pericarditis, as approximately 20% of presenting patients have normal pericardial thickness.⁷ In a retrospective review of 205 consecutive patients, Kim et al⁸ identified echocardiographic features of constriction in 16% of patients after pericardiocentesis, highlighting the diagnostic utility of echocardiography in ECP. The investigators further emphasized that diagnostic features of ECP were present before pericardiocentesis, suggesting that careful TTE interpretation may identify patients at risk for further clinical decompensation who require closer monitoring. Thus, some experts suggest the use of serial limited TTE within 24 hours after pericardiocentesis to monitor for ECP and other complications.⁹

Table 1.

Comparison of Echocardiographic Features of Cardiac Tamponade and Effusive-Constrictive Pericarditis

Echocardiographic Feature	Cardiac Tamponade	Effusive-Constrictive Pericarditis
Pericardial effusion	Present	Present
Respiratory variation in mitral and tricuspid inflow velocities	Mitral >30%, tricuspid >60%	Mitral >25%, tricuspid >40%
Plethoric inferior vena cava	Present	Present
Expiratory hepatic vein diastolic flow reversal	Present	Present
Chamber collapse	Present	Present
Pericardial thickening	Absent	Sometimes
Diastolic septal bounce	Sometimes	Present
Tissue Doppler medial e′ > lateral e′ (ie, annulus reversus)	Absent	Present

In addition to TTE, cardiac magnetic resonance imaging may aid in the diagnosis of ECP and guide treatment decisions. Characteristic findings of ECP on magnetic resonance include septal bounce, reduced pericardial motion, pericardial thickening >4 mm, pericardial inflammation, and complex pericardial effusions.⁵ For some nonpurulent etiologies of ECP, conservative medical therapy can be trialed before surgical management if there are imaging findings suggestive of active pericardial inflammation, such as increased pericardial signal intensity on T2-weighted images, late gadolinium enhancement of pericardium, or pericardial thickening on cine images. Some experts recommend following late gadolinium enhancement to ascertain response to therapy.¹⁰

Guidelines for managing ECP are limited. Overall, treatment depends on the etiology of ECP and the stability of patients. ECP secondary to PP requires pericardial drainage with concurrent use of appropriate antibiotics. Yet with idiopathic or iatrogenic ECP, pericardial intervention may be avoided in close to 50% of patients with conservative management.¹ Similar to acute pericarditis, first-line medical management usually includes the use of nonsteroidal anti-inflammatory drugs and adjuvant colchicine if there are no contraindications. If needed, diuretics should be used cautiously given the preload dependence of patients with ECP. If intervention is required, partial versus complete pericardiectomy should be performed.¹

Follow-Up

At her 1-month outpatient follow-up with the cardiothoracic surgery, infectious disease, and cardiology teams, the patient had a significantly improved clinical status, and antibiotics were discontinued.

Conclusions

ECP is an under-recognized pericardial syndrome that can rapidly complicate PP, with significant hemodynamic sequalae. Serial echocardiography may aid in detecting constrictive physiology after pericardiocentesis. Further studies are needed to guide management.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Visual Summary.

Timeline of the Case

Time	Events
Date of admission/emergent care	A 62-year-old woman presented with chills, shortness of breath, chest pain, and ECG with ST-segment elevation in lateral leads. Emergent coronary angiography showed nonobstructive coronary artery disease.
Day 1	Emergent CT angiogram of the chest showed evidence of large pericardial effusion and no evidence of pulmonary embolism. Initial TTE redemonstrated pericardial effusion, but with no evidence of hemodynamic compromise. Started on treatment for idiopathic acute pericarditis with colchicine and NSAIDs.
Day 7	Patient developed worsening dyspnea, increased oxygen requirement, hypotension, and limited TTE showed worsening pericardial effusion with tamponade physiology. Urgent pericardiocentesis drained 410 mL purulent fluid, improving hypotension and hypoxia. Broad-spectrum antibiotics initiated.
Day 8	Pericardial fluid cultures with heavy growth of Streptococcus pneumoniae. Based on susceptibility results, the patient was de-escalated to targeted antimicrobial therapy with ceftriaxone.
Day 11	Persistent sinus tachycardia and jugular venous distension noted on examination, with repeat TTE with small pericardial effusion but evidence of constrictive physiology.
Day 13	Chest CT redemonstrated a large pericardial effusion and a moderate, loculated left pleural effusion. Patient underwent left-sided chest tube placement. Limited TTE demonstrated persistent constrictive physiology.
Day 15	Patient underwent left video-assisted thoracoscopic surgery (VATS) decortication with chest tube exchange and concurrent partial pericardiectomy.
Day 17	Repeat TTE with only trivial pericardial effusion and no evidence of cardiac tamponade or constrictive physiology.
Day 25	Left chest tube removed.
Day 27	Patient discharged home on oral antibiotic regimen.

CT = computed tomography; ECG = electrocardiogram; NSAIDs = nonsteroidal anti-inflammatory drugs; TTE = transthoracic echocardiogram.